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At 40 years of age, American men and women have a 1 in 5 lifetime risk of the development of heart failure (HF); by the latest estimates, there are 5,700,000 people in the United States who already have a diagnosis of the disease. Moreover, by the year 2030, it is predicted that an additional 3 million Americans will have HF, representing an astounding 25% increase from 2010. Many of these individuals will be older than 65 years of age (1). Clearly, there is an urgent need to identify patients at risk of the development of HF and to initiate effective preventive measures.

What can be done to prevent HF and the resulting personal and societal costs? A first step toward recognizing the importance of risk factors leading to HF came with a shift in classification of HF. Instead of focusing solely on the time-honored New York Heart Association functional classification scheme—a useful method to quantify the degree of functional limitation of the patient with established HF—the American Heart Association (AHA) and American College of Cardiology (ACC) endorsed the use of a staging system focused on both pathophysiology and symptoms (2). The staging system and recommended treatment according to stage are presented in Figure 1 (3). Notably, 2 of the 4 categories, stages A and B, identify patients who are asymptomatic, in an effort to emphasize the need to intervene with proven therapies even before patients become symptomatic with more advanced stages of HF. Stage A represents patients with risk factors for HF, including traditional risk factors for coronary artery disease (CAD) and CAD itself. Stage B represents patients with structural heart disease, including left ventricular hypertrophy or systolic dysfunction, but who remain without HF symptoms. It is still a matter of debate whether asymptomatic diastolic dysfunction is stage A or B. In any case, according to a community-based cohort in Olmsted County, Minnesota, ∼56% of adults older than 45 years of age were classified as stage A (22%) or B (34%). Thus, HF was likely to develop in at least half of this randomly selected Olmsted County population and could be identified before the onset of HF symptoms by medical record abstraction, physical examination, self-administered Goldman SAS questionnaire, echocardiography, and electrocardiography (4).

In this issue of iJACC, Leening et al. (5) suggest an important additional component of the algorithm to predict HF by adding to what is already known about the relationship between coronary artery calcium (CAC) and HF (6,7). In their prospective, cohort study of 1,897 asymptomatic Dutch subjects older than 55 years of age, the authors found a graded association between the extent of CAC, as measured by electron-beam computed tomography, and the risk of incident HF, over a follow-up period of almost 7 years. Remarkably, when corrected for age, sex, and standard cardiovascular risk factors and censoring subjects with incident nonfatal coronary heart disease, a 3-fold increased risk of HF remained, suggesting an association between CAC and HF separate from overt coronary disease in this population (5). Importantly, the Rotterdam cohort was older, so that this study's findings should not be generalized to a younger population or necessarily to one that is more racially diverse, such as the U.S. population, until it is replicated in another source population. We know from previous studies, for example, that differences in CAC exist among ethnic groups (8), although these differences remain poorly understood.

Nonetheless, subjects with increased CAC can be considered to have at least ACC/AHA stage A disease and should be targeted with aggressive strategies to prevent progression to symptomatic disease. One could argue that, on the basis of recent work looking at regional myocardial dysfunction found in asymptomatic subjects, in some of whom HF does develop (9), and the correlation found between areas of CAC and areas of wall motion dysfunction seen on cardiac magnetic resonance imaging (10), these subjects may in fact have subtle structural dysfunction, thereby classifying patients with high CAC scores as ACC/AHA stage B. Regrettably, the Leening et al. (5) study was unable to capture whether HF developed in subjects with reduced or preserved ejection fraction, which may play a role in the pathophysiology of the subsequent development of HF. In future studies, it would be useful to have this distinction. Most importantly, it continues to be evident that we are not doing as much as we can to address and treat standard risk factors, including hypertension, diabetes, obesity, hyperlipidemia, and smoking, using evidence-based measures to prevent HF (11–14). Indeed, it could be argued that spending more money on the identification of HF risk is ill-advised and should rather be spent on the effective management of hypertension, or the prevention of obesity, for a greater number of patients. It has been known for decades that treatment with angiotensin-converting enzyme inhibitors or angiotensin receptor blockers can mitigate the risk of the development of HF (15) or cardiovascular death (16) in patients with stage A and B disease. In addition to our standard risk factor targets, we can now add another marker of risk for incident HF—elevated CAC. Whether assessing CAC as part of the risk stratification scheme for HF is cost-effective or changes patient or physician behavior has yet to be determined. In addition, assessing CAC does have the added disadvantage of radiation exposure, especially compared with a simple blood pressure or lipid assessment. As with the use of CAC for risk stratification for CAD, we have to be sure that the incremental risk reclassification is worth the cost and radiation exposure.

The larger question to be answered in future studies is how do we lessen this risk, above and beyond treatment of standard cardiovascular risk factors? Will our interventions depend on the type of HF (systolic or diastolic) that is involved? Similar to the emerging story with biomarkers, where natriuretic peptides have shown incremental value in predicting the risk of incident HF (17), we need not only an accurate model for prediction, but also proven methods to mitigate the hazard, with a widespread application of prevention measures to our diverse U.S. population.

Footnotes

The authors have reported that they have no relationships relevant to the contents of this paper to disclose.

↵⁎ Editorials published in JACC: Cardiovascular Imaging reflect the views of the authors and do not necessarily represent the views of JACC: Cardiovascular Imaging or the American College of Cardiology.

(2001) ACC/AHA guidelines for the evaluation and management of chronic heart failure in the adult: executive summary: A report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee to revise the 1995 Guidelines for the Evaluation and Management of Heart Failure). J Am Coll Cardiol38:2101–2113.

(2009) 2009 focused update incorporated into the ACC/AHA 2005 Guidelines for the Diagnosis and Management of Heart Failure in Adults: A Report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines Developed in Collaboration With the International Society for Heart and Lung Transplantation. J Am Coll Cardiol53:e1–e90.